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This is why those species more resistant to the damaging effects of reactive oxygen species live longer than their peers. A good example is the naked mole rat, which lives eight times longer than similarly sized rodent species.

With this theme in mind, I noticed an open access paper today that looks at membrane composition differences a little closer to home: in the mitochondria of primates:

The mitochondrial (mt) gene tree of placental mammals reveals a very strong acceleration of the amino acid (AA) replacement rate and a change in AA compositional bias

...

the rate acceleration in the simian lineage is accompanied by a marked increase in threonine (Thr) ... his Thr increase involved the replacement of hydrophobic AAs in the membrane interior [and] analysis reveals a statistical significant positive correlation between Thr composition and longevity in primates.

Even in primates, the composition differences are important - no doubt altering the process of ROS damage and mitochondrial dysfunction that contributes to aging. It reinforces just how central our mitochondria are to aging and longevity, and how vital it is to speed research into repairing damaged mitochondria in humans.

Comments

it is NOT SUFFICIENT to convince me that increasing our peroxidation-resistant membrane lipids would make us live longer: these are only observations/correlations accross species

For instance, SIZE correlates with long life (slightly less convincing) accross species, but within a species short animals often live longer.

Posted by: AgeVivo at October 8, 2008 1:56 AM

I'm not suggesting any changes to the membrane composition. I'm suggesting we periodically repair the damage in mitochondria, and that differential membrane composition is a good illustration as to why repairing that damage will be beneficial.

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